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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [MNase-Seq]

ABSTRACT: Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [MNase-Seq]

PROVIDER: PRJNA833071 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18964300_1.fastq.gz	Fastqsanger.gz
	SRR18964300_2.fastq.gz	Fastqsanger.gz
	SRR18964301_1.fastq.gz	Fastqsanger.gz
	SRR18964301_2.fastq.gz	Fastqsanger.gz
	SRR18964302_1.fastq.gz	Fastqsanger.gz

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [MNase-Seq]

Project description:Transcription factors induce dynamic chromatin reorganization during cell fate transition. Pioneer transcription factors are defined as their capability to engage chromatin by binding to nucleosomal DNA in closed chromatin and inducing chromatin opening. However, it has been also shown that these activities are context dependent. Only a subset of pioneer factors’ binding sites become open and the rest of binding sites remain closed. The molecular mechanisms of this context dependent action are still largely unknown. Here, we explore dynamic chromatin rearrangement during GATA3 dependent mesenchymal-to-epithelial transition (MET) in breast cancer cells. We found site-specific kinetic differences in chromatin binding, nucleosome remodeling and chromatin opening by the pioneer factor GATA3. We also identified that a chromatin remodeling enzyme, CHD4, negatively regulates the GATA3-mediated chromatin opening. The silencing of CHD4 induces abnormal chromatin opening leading to unnecessary gene expression for MET. Our study suggests the active regulation of chromatin potential by the chromatin remodeling enzyme for successful cellular reprogramming.

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ChIP-Seq]

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ATAC-Seq]

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [RNA-Seq]

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [RNA-Seq]

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ChIP-Seq]

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ChIP-Seq]

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ATAC-Seq]

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ATAC-Seq]

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ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

Project description:Glioblastomas (GBM) harbor subpopulations of therapy-resistant tumor initiating cells (TICs) that are self-renewing and multipotent. To understand the regulation of the TIC state, we performed an image-based screen for genes regulating GBM TIC maintenance and identified ZFHX4, a 397-kDa transcription factor. ZFHX4 is required to maintain TIC-associated phenotypes in vitro, suggesting that ZFHX4 regulates TIC differentiation, and its suppression increases glioma-free survival in intracranial xenografts. ZFHX4 interacts with CHD4, a core member of the NuRD (nucleosome remodeling and deacetylase) complex. ZFHX4 and CHD4 bind to overlapping sets of genomic loci and control similar gene expression programs. Using expression data derived from GBM patients, we demonstrate ZFHX4 is a master regulator of CHD4-mediated gene expression. These observations define ZFHX4 as a regulatory factor that links the chromatin remodeling NuRD complex and the GBM TIC state. Examination of binding of ZFHX4 and CHD4 across the human genome, using the 0308 tumor initiating cell line. Two replicates for each protein, compared to whole cell extract inputs.

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Project description:Fibrosis, characterized by sustained activation of myofibroblasts and excessive extracellular matrix (ECM) deposition, is known to be associated with chronic inflammation. RIPK3, a key kinase mediating TNF-driven necroptosis signaling, is upregulated in fibrosis and contributes to the TNF-mediated inflammation. In bile duct ligation-induced liver fibrosis, we found that myofibroblasts are the major cell type expressing RIPK3. Genetic ablation of beta1 integrins, the major profibrotic ECM receptors in fibroblasts, not only abolished ECM fibrillogenesis but also blunted RIPK3 expression via an epigenetic mechanism mediated by the chromatin remodeling factor CHD4. While the function of CHD4 has been conventionally linked to NuRD and ChAHP complexes, we found that CHD4 potently repressed a set of genes, including Ripk3, with high locus specificity but independent of either the NuRD or ChAHP complex. Thus, our data uncover that beta1 integrin intrinsically links fibrotic signaling to RIPK3-driven inflammation via a novel mode of action of CHD4.

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